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Acoustically Reflective Nanoparticles for Tumor Diagnosis
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
R. G. Aswathy, D. Sakthi Kumar
Molecular US imaging is also used for tracking the development of blood vessel (angiogenesis) in tumor tissue and for the validation of effect of drugs on the vascular related diseases. Some of the examples of MBs for the examining of angiogenesis and the progress of anti-angiogenic therapy or chemotherapy include the study with MBs targeted against VEGF/VEGFR-complex, VEGFR2, and endoglin [40]. The molecular US was used for explaining the expression of angiogenic markers in vivo. Cyanoacrylate MBs linked to VEGFR2 and αvß3 integrin binding ligands and quantified the accumulation of MBs in squamous cell carcinoma xenografts in mice based on quantitative volumetric US scanning method. Specificity of targeted MBs was demonstrated by the accumulation of targeted MBs in tumors and variation in expression of markers with matrix metalloproteinase inhibitor treatment was also examined [41]. Significant decrease in marker was observed after the treatment of matrix metalloproteinase inhibitor. Targeted US was beneficial for longitudinal molecular profiling of angiogenesis in tumor and for assessing therapy in in vivo. The dual-targeted MBs integrated with both VEGFR2 and αvß3 integrin have been studied for the improved in vivo imagining of tumor angiogenesis in a human ovarian cancer xenograft tumor model in mice [42].
Bone, Muscle, and Tooth
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
John L. Vahle, Joel R. Leininger, Philip H. Long, D. Greg Hall, Heinrich Ernst
Hyperplasia of the synoviocytes is a commonly observed component of various degenerative or inflammatory conditions and is not typically a primary component. An increased thickness of the synovium has been reported in conjunction with a spectrum of joint and physeal lesions in rodents administered with a matrix metalloproteinase inhibitor (Renkiewicz et al. 2003).
Platelet-mediated shedding of NKG2D ligands impairs NK cell immune-surveillance of tumor cells
Published in OncoImmunology, 2018
Stefanie Maurer, Korbinian Nepomuk Kropp, Gerd Klein, Alexander Steinle, Sebastian P. Haen, Juliane S. Walz, Clemens Hinterleitner, Melanie Märklin, Hans-Georg Kopp, Helmut Rainer Salih
Inhibition of ADAM10 and ADAM17 during culture of tumor cells alone or upon exposure to releasate clearly reduced NKG2DL release, and clearly more pronounced effects were observed with a broad spectrum matrix metalloproteinase inhibitor (MPI) as compared with inhibition of ADAM10 or ADAM17 alone. The finding that the amount of soluble MIC molecules detectable in the presence and absence of releasate declined to a comparable level provides further evidence for the contribution of metalloprotease activity to NKG2DL release upon tumor-platelet interaction (Supplementary Figure 2C).
Current understanding and therapeutic management of contact lens associated sterile corneal infiltrates and microbial keratitis
Published in Clinical and Experimental Optometry, 2021
Lily Ho, Isabelle Jalbert, Kathleen Watt, Alex Hui
Other adjunct treatments have included agents to modulate corneal inflammation and its sequelae. Examples include tetracyclines for their matrix metalloproteinase inhibitor activity to minimise collagenolytic degradation of the cornea stroma;122 amniotic membrane grafts;123 and corneal cross-linking.124 All of these approaches have varied impact and clinical uptake.
Neutrophil peptide-1 promotes the repair of sciatic nerve injury through the expression of proteins related to nerve regeneration
Published in Nutritional Neuroscience, 2022
Fei Yu, Yusong Yuan, Hailin Xu, Suping Niu, Na Han, Yajun Zhang, Xiaofeng Yin, Yuhui Kou, Baoguo Jiang
In this study, b-NGF as well as inflammation-related factors such as IL-1β, IL-10, IL-13, TCK-1 and VEGF were increased after the sciatic nerve injury. The protein b-NGF is an important neurotrophic factor that plays an important role in regulating nerve growth [29]. IL-1β, IL-10, and IL-13 belong to the interleukin family of proteins, which is one of the families most widely studied for its role in stimulating inflammation or anti- or pro-inflammation responses to many diseases [30–32]. TCK-1, also known as CXCL7, is associated with the inflammation of neurons in the brain [33]. VEGF is also strongly associated with inflammation. Inflammatory reactions induced by hypoxia can increase the secretion of VEGF [34]. Inflammation induced by IL-1β can also lead to changes in the levels of pro-inflammatory factors, such as VEGF and IL-6. The sciatic nerve injury also led to increased expression of chemotaxis-related proteins such as B7-2, CINC-2/3, fractalkine and LIX. B7-2 (CD86) is an important costimulatory molecule that participates in the immune response and signal transduction of primary B lymphocytes [35]. Increased expression of B7-2 may participate in the secretion of pro-inflammatory factors, such as TCP-1 and TNF-α, through the presenting function of macrophages [31]. Both CINC-2 and CINC-3 are neutrophil chemokines that can promote the migration and adhesion of neutrophils. Expression at the site of injury may be the main factor affecting the infiltration of neutrophils [36], which are important effectors of acute inflammation [37]. Fractalkine is also an important chemokine [38] that participates in the migration and activation of lymphocytes and phagocytes and regulates pro-inflammatory factors in gram-negative bacterial infection-related diseases [39]. LIX is a chemokine, also known as CXCL5, that plays a regulatory role in inflammation and cancer cell growth caused by cancer metastasis [40]. TIMP-1, which was also increase in the NP-1 and NS groups, is a matrix metalloproteinase inhibitor that plays an important role in the formation of neutrophils. An increase in TIMP-1 can induce an increase in neutrophil levels in mice [41]. Our results showed that a single intermuscular injection of saline did not affect the repair of injured sciatic nerves. Our study suggests that, days after the sciatic nerve crushing injuries in rats, protein factors, such as CINC-2 and LIX, may have caused neutrophils to aggregate at the injured site and induce inflammation. B7-2, TIMP-1, and other proteins could have induced the differentiation of macrophages and granulocytes, leading to further aggregation of macrophages and neutrophils and promotion of inflammation at the injured site. Although both pro- and anti-inflammatory factors were up-regulated, the pro-inflammatory effect of NP-1 may outweigh the anti-inflammatory effect. The secretion of TCK-1 increased, which could have further strengthened the inflammatory response. This subsequently increased the secretion of b-NGF to promote injury repair. VEGF, CINC-3, and fractalkine were not significantly increased over the course of the experiment. Our results indicate that the inflammatory response played a role in the post-injury repair of the sciatic nerve, likely via an increase in b-NGF.